Abstract
Background:
Strength and neuromuscular decrements following knee musculoskeletal injury may accelerate knee osteoarthritis development. This study assessed isometric knee extensor and flexor strength and steadiness between individuals with knee injury, i.e., ligament reconstruction, and knee osteoarthritis to healthy age-matched controls.
Methods:
Four cohorts (1: knee injury and 2: age-matched controls, and 3: radiographic knee osteoarthritis and 4: age-matched controls) were recruited. Participants performed maximal voluntary isometric knee extensor and flexor contractions. Then, strength (e.g., peak and rate of torque development) and steadiness (e.g., peak power, mean, and median frequency) were derived from each raw torque-time curve and associated power spectral density. A Kruskal-Wallis H test and Spearman’s rho correlation analysis assessed cohort differences and association between knee extensor and flexor strength and steadiness.
Findings:
The young adult control and knee injury cohorts exhibited greater knee extensor and flexor strength than the older, knee osteoarthritis cohort (p<0.043). The knee injury cohort, despite being as strong as their healthy counterparts, were significantly less steady with a 92% increase in peak power frequency (p=0.046). The osteoarthritis cohort exhibited 157% less total power compared to the knee injury and young control cohorts (p<0.019). Knee extensor and flexor peak torque, rate of torque development, and mean torque exhibit a significant, positive relation with total power (p<0.018).
Interpretation:
Individuals with knee injury and disease may exhibit weaker or less steady knee musculature, predisposing them to degenerative joint disease. Clinicians may need to restore knee extensor and flexor steadiness to facilitate better joint neuromuscular control.
Keywords: biomechanics, knee, ACL reconstruction, osteoarthritis, steadiness
1. Introduction
Knee musculoskeletal injury, such as anterior cruciate ligament (ACL) tears and concomitant soft-tissue damage, may accelerate the development and progression of degenerative joint disease, such as knee osteoarthritis (OA) (Friel and Chu, 2013; Tayfur et al., 2021). In fact, over 50% of individuals with an ACL reconstruction (ACL-R) exhibit radiographic OA about 7 years after the initial injury (Luc et al., 2014; Tayfur et al., 2021). An ACL tear, with or without surgical intervention, provokes generalized joint instability characterized as joint buckling, shifting, or giving way during weight-bearing activity. This instability may be the result of weaker quadriceps or hamstrings that are critical to dynamic joint stability, and is reportedly a pathogenic factor for OA development and progression (Kamekura et al., 2005; O’Reilly et al., 1998). Individuals with ACL-R and knee OA exhibit quadriceps strength decrements greater than 20% compared to both the unaffected, contralateral limb and healthy counterparts (Lepley, 2015; Palmieri-Smith et al., 2010)Yet, existing research has primarily focused on the individual’s muscle strength or activation decrements, despite the fact that steadiness of the muscle contraction may also provide valuable insight to the underlying joint neuromuscular function and disease progression.
Muscle steadiness, or motor output variability of voluntary movement, describes the precision and control of muscle contraction (Satam et al., 2022). Specifically, evaluating the magnitude and frequency of muscle torque fluctuations during a maximal voluntary isometric contraction (MVIC) depicts the smoothness and accuracy (i.e., steadiness) of muscle contraction (Enoka, 1997; Pua et al., 2010). Individuals with ACL-R reportedly exhibit worse knee extensor contraction steadiness, or higher magnitude and greater frequency of torque fluctuations, compared to age-matched controls (Pua et al., 2015; Spencer et al., 2020). Further, the deficits in knee extensor neuromuscular control that begin following injury reportedly persists up to four years following ACL-R (Goetschius and Hart, 2016; Tayfur et al., 2021). These deficits limit the ability to sustain a consistent, controlled extensor contraction during maximal isokinetic and isometric tasks resulting in a negative influence on rehabilitation, functional performance, and disease progression (Pua et al., 2015, 2010). Steadiness of knee extensor contraction is reportedly related to ACL-R functional outcomes and performance, or persistent movement dysfunction (Pua et al., 2015; Spencer et al., 2020). But, similar relationship for individuals with symptomatic knee OA has not been consistently reported (Satam et al., 2022). In addition, the knee flexors also play a critical role in dynamic joint stability protecting the ACL and other soft-tissue structures. Increases in knee flexor activation reportedly leads to decreased knee extensor steadiness, compromising joint stability and physical performance (Bryant et al., 2009). Yet, functional knee flexor assessment following ACL injury and reconstruction has been primarily limited to traditional muscle strength and activation (or co-activation) metrics, while the impact of ACL-R and OA on knee extensor and flexor steadiness remains relatively unknown.
Assessing knee extensor and flexor torque steadiness in the frequency domain may provide additional context on quantifying joint stability, but to date, has been quite limited. Previous fluctuation analysis has been limited to linear-based calculations that quantify torque around a fixed point within a time series, such as quadriceps force control, torque variability, and torque complexity (Goetschius and Hart, 2016; Perraton et al., 2017; Ward et al., 2019). Muscle force fluctuations, however, reflect an irregular temporal structure and non-linear analyses may be necessary to accurately depict fluctuation content (Slifkin and Newell, 2000). Presently, non-linear assessments of torque complexity, including approximate and sample entropy, have been used in ACL research (Chaney et al., 2023; Johnson et al., 2023), but other frequency domain analyses (i.e., wavelet transformation and power spectral density) for isometric torque-time curves has not been conducted (Czaplicki et al., 2017; Pua et al., 2015; Satam et al., 2022; Tsepis et al., 2004). Adopting frequency domain analyses from other fields, such as techniques previously used to assess brain activity and heart rate variability, may not only bolster our understanding of muscle function in general, but steadiness in particular. For instance, peak power frequency (PPF) has been used to describe muscle torque fluctuation frequency (Satam et al., 2022). But, the inclusion of other frequency domain measures, including mean and median frequency and total power, may be useful in quantifying knee contraction steadiness as well as provide additional context to the fluctuation content and the amount of energy present in the torque-time signal (Phinyomark et al., 2012). Additionally, previous muscle steadiness literature has investigated isokinetic dynamometry to evaluate steadiness through the joint’s full range of motion. However, performing fluctuation analysis on an isokinetic torque-time curve relies upon a changing joint angle, thus, it may not accurately measure the contraction steadiness as the target torque is modulated by different strength outputs at varying joint angles throughout the contraction. Extending the analysis to an isometric contraction may record fluctuations that are representative of neuromuscular deficiencies as the individual could produce completely flat (i.e., steady) torque-time curve once maximum strength is reached. With that in mind, this study sought to assess knee extensor and flexor steadiness during isometric contractions.
The purpose of this study is three-fold: (1) to determine whether knee extensor and flexor muscle strength and steadiness differ between individuals with ACL-R and knee OA to age-matched controls, (2) determine if there is relation between strength and steadiness measures for each muscle group, and (3) whether the strength and steadiness of the knee extensors and flexors are related. We hypothesize that the ACL-R and knee OA cohorts will be significantly weaker and less steady than the healthy counterparts, and there will be a significant linear relationship between and strength and steadiness for both the knee extensors and flexors as well as between the muscle groups.
2. Methods
2.1. Participants
Forty-one adults in four cohorts based on age (1: 12 ACL-R, 2: 8 radiographic knee OA, 3: 13 young adult controls, and 4: 8 older adult controls) participated (Table 1). To be included, participants had to be between 18 and 35 years (ACL-R and young adult controls) or over 55 years (OA and older adult controls). The ACL-R cohort had self-reported previous knee musculoskeletal injury including ACL reconstruction with or without concomitant soft tissue damage, while the OA cohort had physician diagnosed knee osteoarthritis. The control cohorts self-reported no history of physician diagnosed knee musculoskeletal injury or disease. All participants had physician’s clearance to perform physical activity, but those who self-reported recent (in the past six months) pain, injury, or surgery in the back or other lower extremity joints, or any known neurological disorder were excluded. Every attempt was made to match control and clinical participants by age, height, and body mass index. Research approval was obtained from the local Institutional Review Board and all participants provided written consent prior to testing.
Table 1.
Mean (SD) participant demographics for each cohort.
| N | Age (yrs) | Height (m) | Mass (kg) | ||
|---|---|---|---|---|---|
| Young Adults | Controls | 13 | 22.38 (1.94) | 1.75 (0.10) | 73.68 (11.30) |
| ACL-R | 12 | 23.25 (4.00) | 1.71 (0.09) | 78.75 (3.20) | |
| Older Adults | Controls | 8 | 69.00 (3.54) | 1.65 (0.08) | 67.09 (16.21) |
| Knee OA | 8 | 71.13 (4.99) | 1.63 (0.07) | 72.84 (1.93) |
2.2. Experimental Protocol
For testing, each participant had knee extensor and flexor torque measured. Specifically, participants performed three maximal voluntary knee extensor and flexor isometric contractions (MVIC) on an isokinetic dynamometer with a sampling frequency of 100 Hz (HUMAC NORM, CSMI, Stoughton, MA, USA). For each contraction, participants were seated with the hip and knee secured at 90 degrees and 60 degrees, and allowed to grip the dynamometer handles that parallel to seat (Pincivero et al., 2003). Then, participants were asked to maximally extend or flex their knee for 5 seconds three times. Participants were provided 15 seconds of rest between each repetition and a minimum of 40 seconds of rest between the extension and flexion contractions. The repetition with the highest maximal voluntary knee torque was selected for analysis (Satam et al., 2022). Knee strength and steadiness was measured on the dominant limb for the control cohorts (both young and older adults) and on the affected limb for the ACL-R and knee OA cohorts.
2.3. Biomechanical Analysis
Custom MATLAB code (R2023a, Mathworks, Natick, MA) was used to calculate the magnitude and fluctuations of knee extensor and flexor torque. First, to eliminate noise, the torque-time curve representing 80% or greater of the maximum torque was determined to be the area of interest (Pua et al., 2010). From the area of interest, peak torque and rate of torque development (RTD) for knee extension and flexion were recorded as the largest value and maximum slope of the torque-time curve (Nm), respectively (Figure 1A). For analysis, peak torque was normalized to participant body mass (Nm/kg). Average knee extension and flexion strength was calculated by taking the root-mean-square (RMS) of the respective torque-time curve throughout the area of interest (Figure 1A).
Figure 1.

Depicts example raw torque-time curve (A) and associated power spectral density (B) for strength and steadiness analysis.
Each raw torque-time curve was bandpass filtered (2-15 Hz) and linearly detrended to filter physiologic tremors and eliminate signal slope to quantify knee extensor and flexor steadiness (Satam et al., 2022). Using the processed torque-time curve, fluctuation magnitude was calculated as the coefficient of variance (CV), the standard deviation of the filtered torque curve divided by the mean raw torque expressed as a percentage (Satam et al., 2022). To calculate the frequency of torque fluctuations, a Fast Fourier Transform was applied to the filtered torque-time curve to achieve an estimation of signal power spectral density (PSD) (Figure 1B). A Hanning window, with an energy correction factor of 1.63, was applied to increase frequency resolution, reduce spectral leakage between frequencies, and correct for energy distortion created from the window function (Kilby and Prasad, 2013). Peak power frequency (PPF), was calculated as the frequency with the highest power within the torque PSD. Then, mean and median frequency, defined as the product sum of the torque spectral density and frequency divided by the total sum of the signal spectral density, and frequency at which the total power of torque spectral density is split into two equal parts, were calculated, respectively (Phinyomark et al., 2012). Total signal power was calculated as the area under the torque PSD (Phinyomark et al., 2012).
2.4. Statistical Analysis
Muscle strength (peak torque, RTD, and RMS) and steadiness (CV, PPF, mean frequency, median frequency, and total power) of knee extensor and flexor torque were submitted to non-parametric statistical analysis. Normal distribution of each dependent variable was assessed using the Shapiro-Wilk test and data was deemed non-parametric. A Kruskal-Wallis H test assessed cohort (ACL-R, OA, and age-matched controls) differences for each dependent variable. A Bonferroni correction was used for pairwise comparisons. Effect size was calculated using eta squared (η2) and r (ES) for main effects and significant pairwise comparisons according to previous literature (Cohen, 1992). Spearman’s rho (ρ) correlation analysis tested the association between muscle strength and steadiness variables. Alpha was set at p<0.05 and analysis was performed using SPSS v28 software (IMB, Armonk, NY).
3. Results
3.1. Extension
Cohort impacted knee extensor strength and steadiness (Table 2 and Figure 2). Cohort impacted peak torque, RTD, and RMS of knee extensor torque (all: p<0.001, η2=0.385-0.462). ACL-R and young controls exhibited greater peak (p=0.016, ES=0.734; p=0.006, ES=0.656), RTD (p=0.016, ES=0.900; p<0.001, ES=0.656), and RMS (p=0.020, ES=0.835; p=0.001, ES=0.641) of knee extensor torque compared to the OA cohort, while ACL-R cohort also exhibited greater peak torque (p=0.028, ES=0.632) and RMS (p=0.007, ES=0.728) than older adult controls. Cohort also impacted knee extensor PPF (p=0.050, η2=0.131) and total power (p<0.001, η2=0.406). The ACL-R cohort exhibited greater PPF compared to young controls (p=0.046, ES=0.534); whereas, both ACL-R and young control cohorts exhibited greater total power compared to the OA cohort (p<0.001, ES=0.898; p=0.019, ES=0.644).
Table 2.
Mean (SD) for knee extensor strength and steadiness measures for each cohort.
| Peak Torque (Nm/kg)* | RTD (Nm/s)* | RMS (Nm)* | CV (%) | PPF (Hz)* | Total Power (dBm*Hz)* | Mean Frequency (Hz) | Median Frequency (Hz) | ||
|---|---|---|---|---|---|---|---|---|---|
| Young Adults | Controls | 3.01 (0.97) | 2.25 (0.20) | 212.41 (105.42) | 0.57 (0.27) | 11.00 (3.19) | 94.72 (89.10) | 21.11 (6.69) | 15.07 (5.06) |
| ACL-R | 3.23 (0.88) | 2.39 (0.20) | 229.44 (70.63) | 0.59 (0.23) | 29.67 (23.24) | 125.84 (62.49) | 29.32 (12.00) | 29.05 (17.01) | |
| Older Adults | Controls | 1.87 (0.58) | 2.13 (0.29) | 118.70 (63.20) | 0.72 (0.31) | 12.00 (3.46) | 50.88 (45.63) | 19.25 (8.05) | 16.78 (8.90) |
| Knee OA | 1.68 (0.72) | 1.95 (1.12) | 95.18 (36.43) | 0.46 (0.17) | 16.75 (7.69) | 14.96 (10.83) | 22.48 (5.33) | 19.88 (6.89) |
Denotes a significant main effect (p < 0.05) of cohort.
Figure 2.

Mean (SD) for knee extensor (A-C) and flexor (D-F) peak torque, rate of torque development (RTD), and root-mean-square (RMS) for each cohort: young control (blue), ACL-R (orange), older control (grey) and knee OA (black). The asterisk (*) denotes a significant (p < 0.05) difference between each cohort.
Knee extensor strength exhibited a significant relation to steadiness (Figure 3). Peak extensor torque exhibited significant positive relation with RTD (ρ=0.668), RMS (ρ=0.911), and total power (ρ=0.683) (all: p<0.001), while RTD exhibited a positive relation with extensor RMS (ρ=0.792) and total power (ρ=0.656) (both: p<0.001). Knee extensor PPF exhibited significant positive relation with mean (ρ=0.656) and median frequency (ρ=0.746) (both: p<0.001). Knee extensor RMS and CV exhibited a positive relation with total power (ρ=0.754, p<0.001; ρ=0.342, p=0.028) of the knee extensor signal.
Figure 3.

Correlogram depicts the pairwise correlation coefficients among muscle strength and steadiness measures for the knee extensors (A) and flexors (B) through a color scale. The color intensity indicates the strength of the correlation, with positive correlations shown in shades of orange and negative correlations shown in shades of blue.
3.2. Flexion
Cohort impacted knee flexor strength and steadiness (Table 3 and Figure 2). Peak torque (p=0.004, η2=0.282), RMS (p<0.001, η2=0.362), and total power (p=0.034, η2=0.153) for knee flexor torque differed between cohorts. Specifically, the ACL-R cohort exhibited greater peak flexor torque compared to the OA cohort (p=0.043, ES=0.602). ACL-R and young control cohorts exhibited greater flexor RMS compared to clinical older adults (p=0.008, ES=0.721; p=0.021, ES=0.637), while the ACL-R cohort also exhibited greater RMS than older adult controls (p=0.034, ES=0.618). After correcting for type I error, however, there was no significant cohort difference for total power (p>0.05).
Table 3.
Mean (SD) for knee flexor strength and steadiness measures for each cohort.
| Peak Torque (Nm/kg)* | RTD (Nm/s) | RMS (Nm)* | CV (%) | PPF (Hz) | Total Power (dBm*Hz) | Mean Frequency (Hz) | Median Frequency (Hz) | ||
|---|---|---|---|---|---|---|---|---|---|
| Young Adults | Controls | 1.53 (0.56) | 1.95 (0.25) | 111.99 (61.23) | 0.52 (0.16) | 12.54 (5.72) | 10.29 (7.19) | 20.24 (7.44) | 15.79 (6.10) |
| ACL-R | 1.44 (0.38) | 2.00 (0.22) | 104.61 (30.65) | 0.41 (0.34) | 19.00 (13.74) | 15.68 (13.02) | 22.44 (7.81) | 19.31 (11.93) | |
| Older Adults | Controls | 0.98 (0.24) | 1.92 (0.29) | 62.71 (30.65) | 0.50 (0.31) | 17.00 (11.87) | 4.24 (4.33) | 19.05 (8.08) | 15.85 (6.99) |
| Knee OA | 0.97 (0.23) | 1.78 (0.23) | 54.55 (11.27) | 0.45 (0.22) | 13.63 (3.93) | 9.69 (15.05) | 17.12 (4.55) | 14.45 (3.89) |
Denotes a significant main effect (p < 0.05) of cohort.
Knee flexor strength exhibited a significant relation to steadiness (Figure 3). Peak flexor torque exhibited significant positive relation with RTD (ρ=0.396, p=0.010), RMS (ρ=0.867, p<0.001), mean frequency (ρ=0.481, p=0.001), median frequency (ρ=0.345, p=0.027), and total power (ρ=0.368, p=0.018). Knee flexor RTD exhibited positive relation with RMS (ρ=0.542, p<0.001) and total power (ρ=0.468, p=0.002). Knee flexor PPF exhibited negative relation with CV (ρ=−0.576), but positive relation with mean (ρ=0.716) and median frequency (ρ=0.807) (all: p<0.001). Knee flexor RMS exhibited a positive relation with mean frequency (ρ=0.434, p=0.005), while CV exhibited a negative relation with mean (ρ=−0.598, p<0.001) and median frequency (ρ=−0.513, p<0.001). Yet, both RMS and CV exhibited a positive relation with total power (ρ=0.528, p<0.001; ρ=0.452, p<0.001).
3.3. Extension and Flexion Correlations
There was a significant relation between knee extensor and flexor strength and steadiness. Specifically, there was a significant positive relation between extensor and flexor peak torque (ρ=0.819, p<0.001), RTD (ρ=0.462, p=0.002), RMS (ρ=0.887, p<0.001), and total power (ρ=0.469, p=0.002).
4. Discussion
The current study evaluated knee extensor and flexor strength and steadiness for individuals with ACL-R and knee OA. Contrary to our hypothesis, neither ACL-R, nor knee OA individuals exhibited weaker knee musculature than their healthy counterparts. The OA cohort, however, exhibited significantly lower knee extensor strength metrics than the young adult control and ACL-R cohorts. In partial agreement with our hypotheses, the ACL-R, but not knee OA cohort exhibited less steady knee extensors compared to their age-matched controls, while all participants exhibited a significant relationship between knee extensor and flexor strength and steadiness regardless of knee injury or disease.
Unexpectedly, participants with ACL-R and knee OA were not significantly weaker than the healthy counterparts. Although individuals with ACL-R and knee OA reportedly exhibit significant decrements of knee musculature strength up to 20% (Lepley, 2015; Palmieri-Smith et al., 2010), neither the current ACL-R nor knee OA cohorts exhibited a significant decrease in peak knee extensor or flexor strength compared to age-matched controls. Yet, despite being as strong, the ACL-R cohort had a 92% increase in knee extensor PPF, or less steady extensor contraction than the age-matched controls. This decrement in knee extensor steadiness, or increase in frequency content and fluctuation of the knee extensor torque is in line with previous literature for individuals with ACL-R or ACL-deficient knees (Pua et al., 2015; Tsepis et al., 2004), and may contribute to poor neuromuscular control that predisposes these individuals to post-traumatic OA development (Tayfur et al., 2021; Ward et al., 2019). For instance, following ACL-R, individuals purportedly exhibit arthrogenic muscle inhibition and other neuromuscular changes, such as limited motor recruitment, slower motor unit firing rates, and altered conduction velocity that may contribute to the larger, more frequent knee extensor torque fluctuations currently observed (Miljkovic et al., 2015; Nuccio et al., 2020; Sherman et al., 2023). As such, current ACL injury rehabilitation programs reportedly target and may successfully mitigate the muscle atrophy and weakness indicative of arthrogenic muscle inhibition that purportedly increase OA risk following ACL-R (Friel and Chu, 2013; Sherman et al., 2023; Sonnery-Cottet et al., 2019), but may not adequately restore knee extensor steadiness. Considering less steady knee extensors may fail to consistently meet the force requirements of a particular locomotor task, future research is needed to explore whether injury rehabilitation programs that restore contraction steadiness coincide with a beneficial reduction in OA risk.
In agreement with previous literature, the older cohorts exhibited age-related strength decrements (Thompson et al., 2013). Specifically, the older cohorts (knee OA and age-matched controls) exhibited 63% weaker and 99% slower knee extensor torque production compared to the younger ACL-R and their age-matched counterparts. The age-related decrements in peak and RTD of knee extensor torque may be attributed to sarcopenia, or the loss of muscle mass and substantial reduction in fast-twitch muscle fibers associated with normal aging (Miljkovic et al., 2015; Petrella et al., 2005). But, interestingly, the large (up to 44% and 53%) reduction in peak and RTD for knee flexor torque exhibited by the older compared to younger cohorts was not statistically significant. While the reason for the lack of statistical significance for the substantial reduction in magnitude and speed of older adult knee flexor torque production in not immediately evident, the younger cohorts did exhibit a significant 50% to 69% increase in knee flexor RMS, or mean torque throughout the isometric contraction. Therefore, the older individuals’ significant reduction in mean flexor torque may exemplify an age-related decrement in hamstring strength and function that aligns with previous literature (Petrella et al., 2005; Thompson et al., 2013). Considering the hamstrings and the eccentric control of the quadriceps are critical in dynamic knee stability, these age-related muscle decrements may promote joint instability, increasing the risk for degenerative joint disease for older populations (Kamekura et al., 2005; Tayfur et al., 2021). However, future research may be needed to determine if the altered or compromised hamstring function also contribute to disease development.
In agreement with previous literature, knee extensor and flexor strength measures were related. Not surprisingly, participants that produced greater peak knee extensor and flexor torque also exhibited faster (i.e., RTD) and larger mean torque production (i.e., RMS) throughout the respective isometric contraction. Individuals with greater muscle strength possess the natural ability (i.e., underlying neuromuscular capacity) to produce torque faster and sustain higher levels of strength in order to safely complete weight-bearing tasks and reduce injury risk (Rodríguez-Rosell et al., 2018). Knee extensor and flexor strength also exhibited a significant relation to steadiness of the respective muscular contraction. Specifically, all knee extensor and flexor strength measures (peak, RTD, and RMS) exhibited a significant positive relation with total power of the contraction. Considering total power represents the amount of energy in the signal and is modulated by the magnitude of the original torque-time curve, an individual with greater strength also has a more volatile or energized torque signal (Du and Vuskovic, 2004; Phinyomark et al., 2012). Yet, in partial agreement with our hypothesis and previous literature, strength of the knee flexors, but not knee extensors exhibited a relation with frequency shifts on the torque-time curve. In particular, increases in knee flexor strength (peak torque, RTD, and RMS) measures predicted greater contraction steadiness including PPF, mean, and median frequency. Considering a shift in the mean or median frequency is modulated by motor unit recruitment firing rates and conduction velocity (Enoka, 1997; Enoka and Farina, 2021; Sherman et al., 2023), the participants with stronger knee flexors may coincide with faster firing rates and contraction velocity of the knee flexion musculature during isometric contractions. But, conversely, faster firing rates and contraction velocity for both knee extensors and flexors may be related to smaller torque fluctuations, as the magnitude of fluctuations, expressed as CV, showed moderate, negative relation to mean and median frequency. This may reflect the quadriceps or hamstrings failing to consistently reach maximum strength, yet firing faster in attempt to maintain “maximum” isometric torque.
Current novel measures of muscle steadiness, including mean and median frequency and total power, are expansions of frequency domain analysis for assessing muscle fatigue using electromyography (EMG). In EMG analysis, muscle fatigue results in a downward shift on the frequency spectrum with a lower mean and median frequency value compared to a non-fatigued muscle (Phinyomark et al., 2012). This downward shift is largely attributed to changes to motor unit recruitment and function with modulation of recruitment firing rate and fiber conduction velocity, which, as discussed previously, are also physiologic changes observed in individuals following ACL reconstruction (Enoka and Farina, 2021; Nuccio et al., 2020; Sherman et al., 2023). With modulation of recruitment firing rate and fiber conduction velocity resulting in greater torque fluctuations, we expected an upward shift in mean and median frequency during the knee extensor task for the ACL-R compared to healthy controls; however, we found a non-significant 33% and 63% increase in mean and median frequency for the ACL-R cohort, respectively. These findings, in combination with the 92% increase in PPF for ACL-R compared to healthy controls suggests that increases in fluctuation frequency may be specific to a given frequency, rather than distributed across a range of frequencies for the ACL-R cohort. Further, total power, or the first spectral moment of the PSD, relates to the amount of energy in the signal (Du and Vuskovic, 2004; Phinyomark et al., 2012). The OA cohort, which exhibited 157% less total power than the ACL-R and young control cohorts, may produce less fluctuations and signal energy than younger cohorts throughout the respective knee extensor contraction. With no significant difference in fluctuation frequency (PPF, mean and median frequency), the decrease in total power for the OA cohort may be attributed to lower PSD amplitude, which corresponds to weaker muscle contraction or lower signal amplitude. As such, this decrement in total power for the OA cohort may reflect weakness and poor neuromuscular function for the quadriceps and contribute to the progression of OA.
A substantial imbalance of quadricep to hamstring strength (primarily stronger quadriceps) reportedly increases risk of ACL injury and/or reinjury (Acevedo et al., 2014). Yet, understanding the relation of the underlying neuromuscular control between these two muscle groups may provide valuable insight to knee joint function, and be necessary to achieve better clinical outcomes following injury. For instance, both the ACL-R and OA cohorts exhibited, albeit statistically insignificant, imbalance of hamstring-quadriceps strength ratio compared to the heathy controls, which may increase their risk of reinjury or degenerative joint disease development (see Appendix A). In line with previous research, the current experimental outcomes demonstrate a moderate to strong, positive relation between strength characteristics (peak torque, RTD, and RMS) of the knee extensors and flexors (Cossich and Maffiuletti, 2020). While a moderate, positive relation between knee extensor and flexor total power was evident, surprisingly, no significant relation was exhibited between any of the other knee extensor and flexor steadiness measures. As such, the fluctuation magnitude and frequency of isometric torque may be specific to the muscle group. More specifically, the underlying motor unit characteristics responsible for knee joint control during weight bearing activity, including firing rates and conduction velocity, may be muscle dependent regardless of knee injury and disease. Thus, practitioners may need to target the restoration of quadricep and hamstring steadiness independently during injury rehabilitation.
This study may be limited by the low sampling rate of the isokinetic dynamometer. The current sampling frequency of 100 Hz may result in lower frequency resolution within the power spectral density of the torque signal resulting in lower accuracy of frequency content. However, to overcome this limitation during post-processing we applied a Hann window to reportedly increase frequency resolution and reduces spectral leakage between frequencies (Kilby and Prasad, 2013). Regardless, future work recording the torque-time curve at higher sampling frequencies is needed to more accurately depict and quantify muscle steadiness. Additionally, the study participants may be a limitation as we did not control for the time following ACL reconstruction or the severity of knee OA (i.e., Kellgren-Lawrence grade). Testing participants immediately following ACL-R rehabilitation or with severe OA (Kellgren-Lawrence grade > 3 or 4) may present altered neuromuscular function that exacerbates the current strength and steadiness findings for both the quadriceps and hamstrings. Furthermore, we did not control for ACL-R graft type for this cohort (i.e., tendon autografts and allografts) which may influence knee strength and function, or test the non-affected limb which may provide greater insight on the general strength of clinical cohorts. Regardless, we believe the current sample represents the general population for individuals with ACL-R and knee OA.
5. Conclusion
In conclusion, both ACL-R and knee OA individuals exhibited alterations in knee extensor and flexor strength and steadiness that may predispose them to disease development. Specifically, individuals with ACL-R are as strong, but less steady than their healthy, age-matched counterparts; whereas, individuals with knee OA are weaker than both the younger cohorts. The lack of strong, steady muscular contraction, particularly for the quadriceps, is indicative of poor neuromuscular function that may predispose individuals to the development of post-traumatic knee OA and/or contribute to the worsening of knee OA symptoms. During injury prevention and rehabilitation protocols, practitioners may need to expand care beyond quadriceps strengthening to also independently improve the steadiness of a knee extensor and flexor contraction in order to facilitate better neuromuscular control of the knee joint and help mitigate the development and progression of knee OA.
Supplementary Material
Highlights.
Individuals with knee injury are as strong, but less steady than healthy controls.
Individuals with knee osteoarthritis exhibited less signal power than young healthy adults.
A relation between knee strength and steadiness was observed.
Acknowledgements
This study was supported by grants from the NIH National Institute on Aging (R15AG059655) and NIH Institutional Development Awards (IDeA) from the National Institute of General Medical Sciences (P20GM109095, P20GM148321, P20GM103408).
Footnotes
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Conflict of Interest
None of the authors demonstrate any conflict of interest regarding this submission.
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